1. Field of the Invention
The present invention is generally directed to a surgical method for treating glaucoma, and relates more particularly to a method for mechanically altering the insertion angle between the longitudinal ciliary muscle and the scleral spur causing the scleral spur to apply greater tension to the trabecular meshwork thereby opening the meshwork to reduce resistance to outflow of the aqueous humor from the anterior of the eye, thus reducing intraocular pressure.
2. Description of the Prior Art
Glaucoma is a significant public health problem, because it is a major cause of blindness that involves both the central and peripheral vision. Glaucoma is a form of optic neuropathy (a disorder of the optic nerve) that is associated with an increase in intraocular pressure resulting from the eye lacking the ability to relieve the pressure in the anterior chamber of the eye caused by an abnormal buildup in the anterior of the clear fluid known as “aqueous humor.” Aqueous humor, which is formed in the ciliary body in the posterior chamber of the eye at the rate of about 2.5 microliters per minute, enters the anterior chamber through a cleft between the front of the lens and the back of the iris through the pupillary opening in the iris. When the eye is functioning normally, the aqueous humor flows out of the anterior chamber at the same or substantially the same rate it enters and, as result, the pressure in the eye remains safely within the normal range of about 12 to 22 mmHg.
Outflow of aqueous humor from the anterior chamber is by two routes. A minor amount (about 10%) exits through “uveoscleral drainage” between muscle fibers in the ciliary body. This flow is independent of intraocular pressure. However, the major route of outflow is through the trabecular meshwork into Schlemm's canal and is pressure dependent. When this route becomes impeded, the intraocular pressure can become elevated because the inflow of aqueous humor is not balanced until the pressure in the eye rises sufficiently to overcome the impediment to outflow. The result of this increase in pressure is that the pressure is transmitted to the vitreous body which, in turn, presses the retina against the choroid which compresses the blood vessels that feed the retina. In time this can result in loss of vision, both peripheral and central, and eventually lead to complete blindness.
Raised intraocular pressure is the most important and the only clinically modifiable risk factor for glaucoma currently available. The clinical treatment of glaucoma is typically approached in a step-wise fashion. Medication often is the first treatment option. Administered either topically, the most common approach, or sometimes orally, the medications used to treat glaucoma work to either reduce aqueous production or to increase outflow. Currently available medications have many serious side effects including: congestive heart failure, respiratory distress, hypertension, depression, renal stones, aplastic anemia, sexual dysfunction and death. Compliance with medication is also a major problem, with some estimates that over half of glaucoma patients do not follow their correct dosing schedules. In one study by an HMO, half of patients surveyed did not fill the prescription the first time and one-fourth failed to do so the second time. Compliance is also complicated by the fact that, in the early stages at least, patients with glaucoma may be asymptomatic.
When medication fails to adequately reduce the pressure, a variety of surgical techniques can be employed. Generally these include canaloplasty, laser trabeculoplasty, trabeculectomy, and the insertion of shunts. Generally these surgical interventions provide only temporary relief from elevated intraocular pressure and disease progression can resume. Accordingly there remains a substantial need for improved treatments for glaucoma, particular ones that are not medication regimens requiring strict patient compliance or surgical techniques that are only temporarily successful.